Mechanism(s) of mitochondrial hyperoxidation after global cerebral ischemia

Advances in Experimental Medicine and Biology

Volumn 471, Issue , 2000, Pages 175-180

  Perez Pinzon, M A ^a   Sick, T J ^a   Rosenthal, M ^a  

^a UNIVERSITY OF MIAMI MILLER SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE;

BRAIN INJURY; BRAIN ISCHEMIA; CELL DAMAGE; CELL DEATH; CONFERENCE PAPER; ELECTRON TRANSPORT; FLUORESCENCE IN SITU HYBRIDIZATION; HIPPOCAMPUS; HOMEOSTASIS; HUMAN; HUMAN TISSUE; OXIDATION; OXIDATION REDUCTION REACTION; PRIORITY JOURNAL; REOXYGENATION; RESPIRATORY CHAIN;

ANIMALS; BRAIN ISCHEMIA; CYTOCHROME C GROUP; HIPPOCAMPUS; MITOCHONDRIA; OXIDATION-REDUCTION; RATS;

EID: 0034463699     PISSN: 00652598     EISSN: None     Source Type: Book Series    
DOI: None     Document Type: Conference Paper

References (26)

1. Ischemic delayed neuronal death: A mitochondrial hypothesis
2. Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function
3. The permeability transition pore as a mitochondrial calcium release channel: A critical appraisal
4. Postischemic inhibition of cerebral cortex pyruvate dehydrogenase
5. The respiratory chain and oxidative phosphorylation
6. The mitochondrial permeability transition pore is modulated by oxidative agents through both pyridine nucleotides and glutathione at two separate sites
7. Oxygen sensitivity of mitochondrial redox status and evoked potential recovery, early during repeffusion in post-ischemic rat brain
8. +2 and potentiates release of cytochrome c
9. Free radicals in CNS injury
10. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
11. Oxygen radicals in CNS damage
12. Metabolic, ionic, and electrical responses of gerbil brain to ischemia
13. Release of mitochondrial aspartate aminotransferase (mAST) following transient focal cerebral ischemia suggests the opening of a mitochondrial permeability transition pore
14. Antioxidants, mitochondrial hyperoxidation and electrical activity recovery after anoxia in hippocampal slices
15. Calcium influx from the extracellular space promotes NADH hyperoxidation and electrical dysfunction after anoxia in hippocampal slices
16. Prolonged anoxic depolarization exacerbates NADH hyperoxidation and promotes poor electrical recovery after anoxia in hippocampal slices
17. Cytochrome c is released from mitochondria into the cytosol after cerebral anoxia or ischemia
18. Mitochondrial hyperoxidation signals residual intracellular dysfunction after global ischemia in rat neocortex
19. Mitochondrial hyperoxidation after cerebral anoxia/ischemia: Epiphenomenon or precursor of residual damage?
20. Measurement of metabolic activity associated with ion shifts
21. Mitochondrial dysfunction in ischaemia-reperfusion
22. Altered mitochondrial respiration in selectively vulnerable brain subregions following transient forebrain ischemia in the rat
23. Cerebral glucose metabolism during the recovery period after ischemia-its relationship to NADH-fluorescence, blood flow, EcoG and histology
24. Effect of peroxide, sodium, and calcium on brain mitochondrial respiration in vitro: Potential role in cerebral ischemia and reperfusion
25. NADH fluorescence and regional energy metabolites during focal ischemia and reperfusion of rat brain
26. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked